How Kidney Stones Form and What Raises Your Risk

Kidney stones form when dissolved minerals in your urine become so concentrated that they crystallize, clump together, and grow into solid masses too large to pass painlessly. The underlying driver is something researchers call supersaturation: when there is more of a mineral in your urine than the liquid can hold in solution, crystals begin to precipitate out, much like sugar crystallizing at the bottom of an over-sweetened glass of iced tea. What tips someone from “concentrated urine” to “actual stone” depends on a surprisingly long list of factors, from what you eat and drink to the bacteria living in your gut, the climate you live in, and even the time of day.

From Supersaturation to Stone

The process begins with urine chemistry. Your kidneys filter waste products and excess minerals from the blood, concentrating them in urine for disposal. When the concentration of stone-forming substances like calcium, oxalate, phosphate, or uric acid climbs above a threshold, the urine becomes supersaturated, and tiny crystals start to form.¹ Whether those crystals become a stone depends on a tug-of-war between promoters (substances that encourage crystal growth and aggregation) and inhibitors (substances that block it). Citrate, magnesium, and certain urinary proteins normally act as brakes, keeping crystals small and washable. When the balance tilts toward promotion, crystals grow, stick together, and anchor themselves inside the kidney.

Both genetic and environmental factors push that balance. High supersaturation, driven by diet, hydration, metabolic conditions, or inherited traits, leads to crystallization in the tiny collecting ducts at the tips of the kidney’s inner structures. Crystals can plug the openings of those ducts into the kidney’s drainage basin and continue growing as fresh supersaturated urine flows over them.²

Randall’s Plaques and the Anchoring Problem

For the most common type of kidney stone, calcium oxalate, there is a specific anchoring mechanism that researchers have studied in detail. Deep inside the kidney’s tissue, tiny deposits of calcium build up in the walls surrounding the loops of Henle, the hairpin-shaped tubes that concentrate urine. These mineral deposits start in the basement membrane of the ascending thin limbs of these loops and spread outward through the surrounding tissue toward the inner surface of the kidney.³ The resulting mineral buildup is called a Randall’s plaque, named after the surgeon who first described them in the 1930s.

When the tissue lining the kidney’s inner surface erodes or breaks down, a Randall’s plaque gets exposed to urine. Proteins from the urine coat the exposed surface, and crystals in the supersaturated urine begin to attach. Layer by layer, alternating bands of mineral and organic material accumulate until crystallization outpaces the body’s protective mechanisms and a full calcium oxalate stone begins to form on top of the plaque.⁴ Large amounts of Randall’s plaque are unique to people who form calcium oxalate stones without an identifiable secondary cause, which is the most common stone-forming scenario. In this population, the plaque effectively acts as a foundation that the stone builds upon.⁵

Not All Stones Are the Same

Kidney stones come in several varieties, and understanding the type matters because each has a different chemistry and a partly different set of risk factors.

• Calcium oxalate: The most common variety by far, accounting for the majority of stones. These grow on Randall’s plaques and are driven by high urinary calcium and oxalate concentrations.
• Calcium phosphate: Favored by higher urinary pH and lower citrate levels. A study comparing calcium phosphate stone formers with calcium oxalate stone formers found that a modest rise in urine pH or a drop in citrate each roughly doubled the odds of forming a calcium phosphate stone instead.⁶
• Uric acid: Formed primarily because urine is too acidic, not necessarily because uric acid levels are abnormally high. Low urinary pH is the chief risk factor, with low fluid intake and excess uric acid playing secondary roles.⁷⁸
• Struvite: These form when certain urease-producing bacteria infect the urinary tract, splitting urea into ammonia and raising urine pH dramatically. The alkaline environment causes magnesium ammonium phosphate crystals to precipitate. Laboratory experiments confirm that bacteria like P. aeruginosa and E. cloacae directly control the nucleation and shape of struvite crystals.⁹
• Cystine: A rarer type caused by an inherited condition in which the kidneys leak excessive amounts of the amino acid cystine into the urine, where it crystallizes.

Stone composition has also been shifting over time. An analysis of over 11,000 stones spanning two decades found that the proportion of stones from women rose significantly, and among women, uric acid stones became more common while struvite stones dropped sharply, likely reflecting changes in urinary tract infection management and rising rates of metabolic conditions.

How Fluid Intake Shapes Your Risk

Dilution is the simplest defense against supersaturation. When you drink more fluid, your urine volume goes up, which lowers the concentration of every stone-forming substance in it. A systematic review spanning two decades of research found a consistent link between higher fluid intake, greater urine output, and reduced stone formation.¹⁰ A dose-response analysis put numbers to it: each additional 500 milliliters of water per day was associated with about a 7 percent lower risk of forming a stone, and the general target for protection appears to be producing at least 2.5 liters of urine daily.¹¹

The type of fluid may also matter. That same analysis found that increased consumption of tea and alcohol was associated with reduced kidney stone risk, though the mechanisms are not entirely settled. Sugar-sweetened beverages, on the other hand, have been linked to increased risk in some cohort studies, possibly because fructose can raise uric acid excretion.

Diet Beyond Hydration

A common misconception is that people who form calcium stones should avoid calcium in their diet. The evidence points in the opposite direction. Adequate dietary calcium, taken with meals, binds oxalate in the gut and prevents it from being absorbed into the bloodstream. Cutting calcium from your diet can actually increase the amount of oxalate that reaches your kidneys and raise stone risk.¹² The key is to get calcium from food rather than supplements taken between meals, since timing it with oxalate-containing foods is what makes the binding happen.

High sodium intake is a well-recognized risk factor. When you excrete more sodium in your urine, your kidneys also dump more calcium, raising supersaturation. Sodium restriction is standard advice for stone prevention for this reason.¹²

Animal protein is another contributor. A study comparing a vegetarian diet to a high-animal-protein diet found that urinary calcium excretion rose roughly 50 percent on the animal protein diet. That diet also made urine more acidic, increasing the amount of undissociated uric acid, and it lowered citrate excretion, removing one of the body’s natural stone inhibitors.¹³ In other words, a meat-heavy diet hits stone risk from three angles at once: more calcium in the urine, more uric acid, and less of the citrate that normally keeps crystals in check.

Medical Conditions That Raise the Odds

Kidney stones are increasingly understood as part of a web of metabolic problems rather than an isolated event. Stone formers face higher rates of chronic kidney disease, bone loss, coronary artery disease, high blood pressure, and type 2 diabetes.¹⁴ Whether the stones cause some of these problems, share a common metabolic root with them, or both, is still being worked out. But the association is strong enough that a kidney stone should probably prompt your doctor to check for metabolic risk factors beyond the urine.

Obesity is a particularly important driver. Rising obesity rates track with rising stone rates, and the relationship has physiological explanations: excess body weight is linked to more acidic urine, higher calcium excretion, and insulin resistance, all of which favor stone formation.¹⁵ Inflammatory bowel disease is another medical risk factor, especially Crohn’s disease, because chronic intestinal inflammation increases oxalate absorption. When the gut cannot properly handle bile salts and fatty acids, more oxalate gets through the intestinal wall and into the bloodstream, leading to high urinary oxalate and a greater chance of calcium oxalate stones.¹⁶ Bariatric surgery, especially gastric bypass, produces a similar effect by rearranging the gut’s absorptive landscape.

Medications as an Overlooked Cause

Some drugs can directly cause kidney stones, and they fall into two categories. The first group includes poorly soluble drugs that are heavily excreted by the kidneys and can crystallize in the urine themselves. The second group includes medications that do not form stones on their own but shift your urine chemistry in ways that promote stone formation, such as altering urinary pH or increasing the excretion of calcium, phosphate, oxalate, or uric acid.¹⁷ Common examples in the first category include certain protease inhibitors used in HIV treatment and some antibiotics. In the second category, topiramate (a seizure and migraine drug) is a well-known offender because it inhibits an enzyme that affects urine pH and citrate levels. If you have a history of stones and are starting a new medication, it is worth asking whether the drug has any known lithogenic effects.

Your Gut Bacteria May Be Protecting You

One of the more surprising discoveries in kidney stone research involves a gut bacterium called Oxalobacter formigenes. This microbe specializes in breaking down oxalate in the intestine, which means less oxalate gets absorbed into the blood and less ends up in the urine. A case-control study found that colonization with O. formigenes was associated with about a 70 percent lower risk of being a recurrent calcium oxalate stone former.¹⁸ Roughly 38 percent of healthy non-stone-formers in that study carried the bacterium, compared to only 17 percent of stone formers.

Antibiotics are a likely culprit behind the loss of O. formigenes, since the bacterium is susceptible to many commonly prescribed drugs. Research has confirmed that antibiotic courses can wipe out O. formigenes colonization, and once it is gone, it may not come back on its own.¹⁹ This raises the uncomfortable possibility that routine antibiotic use earlier in life could permanently raise stone risk by depleting a protective member of the gut microbiome. Probiotic strategies to restore O. formigenes are being explored, but none are in routine clinical use yet.

Beyond O. formigenes, your urine itself contains proteins that actively inhibit crystal formation. A proteomic study identified at least 16 proteins consistently present in the most potent crystal-inhibiting fractions of normal urine, including five with well-documented anti-stone activity. Many of these proteins are found at lower levels in the urine of people who form stones compared to healthy individuals.²⁰ The body, in other words, has a built-in defense system against crystallization, and variations in that system help explain why two people with similar diets can have very different stone histories.

Climate, Heat, and the Stone Belt

Urologists have long noticed that kidney stones are more common in warmer regions and during summer months. A systematic review of studies from the United Kingdom, South Korea, the United States, Saudi Arabia, Italy, Japan, and several other countries found a consistent link between higher monthly mean temperatures and higher rates of kidney stone events.²¹ The mechanism is straightforward: heat causes sweating, sweating reduces urine volume, and reduced urine volume raises supersaturation.

The effect appears to be fast-acting and nonlinear. A study modeling kidney stone presentations in South Carolina found that the risk of presenting with a stone increased in the two days following a temperature event, with no ceiling effect at higher temperatures, meaning the hotter it got, the worse the risk became.²² Climate projections suggest that warming temperatures will push more of the country into “stone belt” territory, a term traditionally used for the southeastern United States where stone rates are highest.

When Stones Form During the Day

Your urine chemistry is not constant throughout the day, and those fluctuations influence what kind of stone you are at risk for. Studies of stone patients have found distinct daily pH patterns depending on stone type. People who form uric acid stones tend to have low urinary pH around the clock, creating a persistently acidic environment that favors uric acid precipitation. People who form mixed calcium oxalate and calcium phosphate stones, by contrast, have pH that dips low in the early morning hours but rises during the day.²³²⁴

Calcium excretion also follows a daily rhythm, peaking in mixed-stone patients and staying low in uric acid stone patients. These patterns have practical implications. Collecting a single 24-hour urine sample, the standard test for evaluating stone risk, blends all these peaks and valleys into an average that can mask the real trouble spots. Research into shorter collection windows that capture the high-risk periods has shown that typical circadian rhythms exist for all stone-forming substances in urine, and “peaks” in excretion can be hidden when you only look at the 24-hour average.²⁵ Hydrating before bed, when urine concentrates most, is one low-tech way to address the overnight risk window.

Identifying Stones Without Surgery

Once a stone forms, knowing what it is made of matters for treatment and prevention. Traditionally, stone composition was determined only after it was removed or passed, through chemical or infrared analysis. Dual-energy CT scanning has changed that by allowing radiologists to distinguish stone types before any procedure. The technique uses two different X-ray energy levels to characterize the material based on how it absorbs each one. A study of 227 kidney stones found that dual-energy CT correctly classified 225 of them, with pooled accuracy around 99 percent.²⁶ Further refinement using spectral analysis has proven especially useful for mixed-composition stones, which are common and harder to classify.²⁷

Knowing stone composition before treatment matters practically. A uric acid stone, for example, can often be dissolved by alkalinizing the urine with potassium citrate, avoiding surgery entirely. A calcium oxalate stone cannot be dissolved that way and may require shock-wave lithotripsy or ureteroscopy. Struvite stones demand not just removal but treatment of the underlying urinary tract infection to prevent regrowth. Getting the composition right up front lets doctors and patients skip unnecessary procedures and tailor prevention strategies to the specific chemistry driving the problem.